American Scientist

WESTERN DISEASES: An Evolutionary Perspective. Tessa M. Pollard. xii + 223 pp. Cambridge University Press, 2008. $65.

Economic development, it would seem, is good for your health. In general, life expectancy correlates quite tightly with gross domestic product (GDP) or per capita income. Richer countries have, on average, lower rates of infant mortality, better health-care infrastructure and more advanced medical technologies than are available in the developing world. But the correlation between wealth and well-being is not as simple as one might think. When GDP is plotted against life expectancy, the resulting curve (often called the “Preston curve” after Samuel H. Preston, who first discovered this correlation) shows some interesting features. In particular, life expectancy rises sharply with income only until per capita GDP reaches about $4,000; after that, the rate of increase becomes much more modest. Above $15,000 or so, the gains in life expectancy slow further; it increases by only four years as per capita GDP rises from $15,000 to $25,000. Any gains beyond that point are almost indiscernible.

Why is the relationship between wealth and health not linear? A number of explanations have been put forth. The shape of the flattening curve may be controlled by the upper limit of human life expectancy. Moreover, longer life expectancies in countries with low GDPs are usually achieved through reductions in infant mortality.

But there’s a different category of explanation: the argument that new diseases—cardiovascular disease, cancer and asthma, among others—become prevalent as countries grow wealthier, thus putting another upper limit on life expectancy. These diseases of the rich push back against the benefits conferred by increasing GDP, eventually causing the Preston curve to taper off. These maladies of affluence are responsible for much of the morbidity and mortality seen in the developed world.

The book Western Diseases explores from an explicitly evolutionary viewpoint the noncommunicable diseases that are on the rise in developed nations of the West. Author Tessa M. Pollard argues that modern Homo sapiens evolved in and adapted to environments far different from the ones in which we find ourselves today. Because of that, our physiology, honed in a world of small population groups, scarcity and episodic plenty, now betrays us. The modern world—sedentary, urbanized and, for many, extraordinarily rich in calories—has turned former adaptations into liabilities. Moreover, Pollard suggests, we will have to accept this evolutionary perspective in order to make any improvement in health indicators and outcomes.

The notion that we have been shaped by our evolutionary history seems so self-evident as to not need reiterating. All life is the product of its past. Pollard argues, as have many others before her, that the vast array of important noncommunicable disorders experienced in developed nations can be understood as the result of ancient adaptations gone awry in modern environments. A chapter devoted to obesity, type 2 diabetes and cardiovascular disease is followed by one discussing the debate over “thrifty genotypes” versus “thrifty phenotypes”; a chapter on reproductive cancers is followed by one on reproductive function, breastfeeding and menopause; and asthma and allergic disease share a chapter, as do depression and stress. Bringing up-to-date epidemiological, physiological and comparative data to bear on her analysis of increasing disease rates, Pollard argues persuasively that these seemingly disparate noncommunicable diseases all come about through the mismatch between our ancient selves and our modern circumstances.

All of the chapters are interesting, but the sections dealing with cardiovascular disease and type 2 diabetes are the most compelling. Here Pollard develops a particularly nuanced case for the benefits of an evolutionary approach, paying careful attention to the ongoing debate between the “thrifty genotype” and the “thrifty phenotype” as explanations for the obesity epidemic sweeping the developed and developing world.

The genotypic hypothesis argues that selection favored Paleolithic hunter-gatherer genotypes that quickly released insulin following the consumption of a large meal (a rare event). This broad and somewhat vague hypothesis has collided with findings from detailed field studies showing that contemporary hunter-gatherer cultures do not experience extended periods of caloric deprivation. More recent modifications of the original hypothesis have emphasized particular environmental variables that could select for nonthrifty genotypes, and specifically for increased insulin sensitivity; these factors include the introduction of foods rich in simple sugars into the diet of certain cultures. In this formulation, selection preserved thrifty genotypes in all but a few populations in which changes in cultural practices or environments gave nonthrifty genotypes the upper hand. These are all plausible scenarios. But to her credit, Pollard subjects the popular genotypic explanations to critical scrutiny and finds them wanting.

In contrast, the thrifty phenotype hypothesis maintains that when nutritional resources are in short supply, a fetus will adapt, and the result will be a smaller body size and a lower metabolic rate. If this individual undergoes an abrupt change in nutritional status later in life, he or she will be at increased risk of becoming obese and developing diabetes. An abrupt change in nutritional environment is characteristic of the process of westernization and may help account for the recent dramatic rise in type 2 diabetes (and other diseases) in many parts of the world.

As Pollard acknowledges, any evolutionary explanation for noncommunicable illnesses must address the fact that all of us can trace our ancestry back to East Africa, as well as the fact that we are a young species. Yet despite our shared and recent ancestry, the incidence of many of the conditions discussed in Western Diseases varies significantly from one population to another. It’s a vexing issue, which deserves the attention Pollard gives it.

Although the appeal to evolutionary logic is inherently compelling, such arguments need to be handled with care. This book paints a picture of ancestral hominins (humans and their immediate ancestors) exquisitely adapted to their hunter-gatherer environments, thrust suddenly and unexpectedly into the sedentary, high-density environments that followed on the heels of the invention of agriculture. But this perspective appears strangely romantic, harkening back to a Rousseau-like Eden where our ancestors lived in perfect balance with their surroundings. Compelling as the vision might be, there is little evidence to suggest such long-term harmony. The hallmark of the hominin lineages—the ability to use language, tools and imagination to construct and manipulate the environment—virtually guaranteed constantly changing environments, as did climatic fluctuations over the past 2 million years.

Furthermore, as Pollard herself concedes, humans continue to evolve, culturally and biologically, in response to their fluid environment. To be sure, changes over the past 200 years have been unprecedented in both their magnitude and speed. In those 10 generations, there has been little time for genetic change to accumulate. But the vision of a fully adapted past and a completely maladaptive present requires drawing a sharp line across a continuum of evolutionary change.

Throughout our history as a species, our biology and our cultural practices have adapted to changing environments, and that process is ongoing. Still, Western Diseases persuades us that we can only understand health and disease in an evolutionary context. Alas, it also reminds us that you can’t fool Mother Nature—or Papa Evolution.

Robert L. Dorit is an associate professor in the Department of Biological Sciences at Smith College. His work focuses on experimental evolution of molecules and bacteria, and on the design of novel antibiotics.